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首页> 外文期刊>The European Journal of Neuroscience >Phasic bursts in rat magnocellular neurosecretory cells are not intrinsically regenerative in vivo.
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Phasic bursts in rat magnocellular neurosecretory cells are not intrinsically regenerative in vivo.

机译：大鼠大细胞神经分泌细胞中的阶段性爆发在体内不是固有再生的。

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Abstract Vasopressinergic hypothalamic magnocellular neurosecretory cells fire in phasic bursts. Burst initiation involves summation of postsynaptic potentials to generate action potentials. Action potentials are each followed by a nonsynaptic depolarizing after-potential that summates temporally to generate a plateau potential and so sustain activity throughout the burst. It is unknown whether this plateau potential exceeds spike threshold in vivo to cause intrinsic regenerative firing or simply approaches threshold to increase the probability that excitatory postsynaptic potentials will trigger further action potentials. Here we show that pharmacological blockade of ionotropic glutamatergic transmission by microdialysis application of kynurenic acid into the supraoptic nucleus of anaesthetized rats prevents spontaneous bursts and bursts (after-discharge) evoked by short trains of antidromically stimulated action potentials in magnocellular neurosecretory cells. Even during prolonged depolarization induced by 1 m NaCl infusion, kynurenic acid microdialysis application still blocked after-discharge. The ability of kynurenic acid to block after-discharge during osmotic stimulation was not caused by an unmasking of inhibitory postsynaptic potentials as kynurenic acid was equally effective in the presence of the ionotropic gamma-aminobutyric acid receptor antagonist, bicuculline, nor did it result from inhibition of plateau potential amplitude as this was unaffected by kynurenic acid and bicuculline in vitro, as was after-discharge evoked in vitro. We conclude that phasic bursts are nonregenerative in vivo but rather require continued excitatory synaptic input activity superimposed upon a subthreshold plateau potential to sustain burst activity.
机译：摘要加压素能刺激下丘脑大细胞神经分泌细胞分阶段爆发。爆发起始涉及突触后电位的总和以产生动作电位。每个动作电位后接一个非突触去极化后电位，该电位暂时累加以产生平稳电位，从而在整个爆发过程中维持活动。尚不清楚该平台电位在体内是否超过峰值阈值以引起内在的再生激发，或者仅仅是接近阈值以增加兴奋性突触后电位将触发进一步动作电位的可能性。在这里，我们显示了通过将微缩尿嘧啶酸注入透析大鼠的视上核中，通过微透析将离子型谷氨酸能传递的药理作用阻止了自发性猝发和短时训练的麻痹性神经分泌细胞中抗屈光刺激的动作电位引起的猝发（猝发后放电）。即使在因注入1 m NaCl而引起的长时间去极化过程中，犬尿酸的微透析应用仍会阻止放电后的放电。在渗透性γ-氨基丁酸受体拮抗剂双小分子存在下，犬尿酸同样有效，犬尿苷酸在渗透刺激过程中阻止放电后释放的能力并不是由抑制突触后电位引起的。平台电位振幅的变化，因为在体外不受屈尿酸和双瓜氨酸的影响，在体外诱发的放电后也是如此。我们得出结论，阶段性爆发是体内非再生的，而是需要持续的兴奋性突触输入活动叠加在低于阈值的高原电位上来维持爆发活动。

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